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Updates in Therapeutics 2015:
The Pharmacotherapy Preparatory Review &
Recertification Course
Fluids, Electrolytes, and Nutrition
Leslie A. Hamilton, PharmD, BCPS
University of Tennessee, Knoxville, TN
Updates in Therapeutics® 2015:
Agenda
Distribution of Total Body Fluid
Fluid resuscitation vs. Maintenance IV Fluid
Crystalloid vs. Colloid
Osmolarity of IV Fluids
Hyponatremia and Hypertonic SalineHyponatremia and Hypertonic Saline
Hypotonic Fluid
Hypernatremia
Hypo and Hyperkalemia
Other Electrolytes and Shortages
Enteral and Parenteral Nutrition
Self-Assessment Question #1: Fluids
� 74 yo female with cough, temp 102, and lethargic
� BP 72/40, HR 115, UO 10 ml/hr, WBC 18K, Cr 1.7
(baseline 1.2), wt 72kg
� After 500 mL NS IV bolus, BP 80/46, HR 113� After 500 mL NS IV bolus, BP 80/46, HR 113
� CXR – pneumonia
� PMH – CAD, arthritis
Page 2-4
Which is the best treatment option?
A. Furosemide 40mg IV
B. 5% albumin 500 mL + NE for SBP > 90
C. 1000ml bolus with D5W/0.9% NaClC. 1000ml bolus with D5W/0.9% NaCl
D. 1000ml bolus with 0.9% NaCl
Page 2-4
To answer Self-Assessment Question
#1, think about:
� How do we recognize intravascular volume
depletion?
� How do IV fluids distribute into total body fluid?
What IV fluids can be used to optimize � What IV fluids can be used to optimize
intravascular volume?
Total Body Fluid
60%
Intracellular (IC)
40%
Extracellular (EC)
75% Interstitial (IS)
25% IntravascularPage 2-7
Intravascular Space
� Not exactly “extracellular” because there are cells
in this space (RBC’s)
� Plasma is the extracellular fluid in the
intravascular space (about ~ 3L) intravascular space (about ~ 3L)
� An additional ~ 2L of fluid in RBC’s, making the
total blood volume about 5L
� Intravascular fluid is analogous to the fluid in
your car’s gas tank
Page 2-7
Distribution of IV Crystalloid
0.9% NaCl, LR, Normosol
Na+ and Cl+ do not freely enter cells
Evenly distribute in EC
Each L provides 250 mL into intravascular space
D5W
Dextrose is metabolized to H2O and CO2
Water crosses any membrane
Each L provides 100 mL into intravascular space
Page 2-8
Distribution of IV Colloid
� Colloids are theoretically too large to cross capillary
membrane
� 500 mL infused provides 500 mL intravascular volume
replacement
� PRBC
� Pooled human plasma (albumin 5%, plasma protein
fraction or plasmanate)
� Semi-synthetic glucose polymers (dextran)
� Semi-synthetic hydroxyethyl starch (hetastarch)
Page 2-8
Distribution of IV Colloid
� Unlike 5% albumin, 25% albumin will result in
volume expansion 5x the volume administered
� 100 mL 25% albumin results in 500 mL intravascular
volume replacement.volume replacement.
� Use caution because fluid redistribution can cause
cellular dehydration
� May be useful in patients with ascites or pleural
effusions where fluid redistribution is the goal
Page 2-8
Fluid Resuscitation� Intravascular fluid depletion commonly due to:
� Hemorrhagic shock
� Septic shock
� S/S usually occur when 15% (~750 mL) lost
� Hypotension, tachycardia, ↓ UO, reduced CO and organ
hypoperfusionhypoperfusion
� Improvement after fluid bolus
� Need prompt intravascular fluid replacement
� Through a central venous catheter
� Administer as a 500 – 1000 mL bolus, reassess and
continue as long as S/S are improving
Page 2-8
Crystalloids vs. Colloids
� Crystalloids (NS, LR, Normosol) are recommended
� LR is historically used in trauma patients
� Lactate is metabolized to bicarbonate (theoretically
useful for metabolic acidosis)
No evidence of superiority over NS� No evidence of superiority over NS
� Colloids may seem better than crystalloids based
on distribution properties
� No evidence to demonstrate improved outcomes
� Higher cost
Page 2-9
Colloids: Popular but Controversial
� Consider albumin after fluid resuscitation with
crystalloid (usually 4 – 6 L) has failed to achieve
hemodynamic goals or when clinically significant
edema limits further administration of crystalloid
� e.g., Pulmonary edema causing hypoxia� e.g., Pulmonary edema causing hypoxia
� Consider albumin if level < 2.5 and require large
volumes of crystalloid
� Avoid hetastarch
Page 2-9
� Consider albumin (preferably 25%) with loop
diuretics in patients with:
� Clinically significant edema AND
� Albumin concentration < 2.5 (in whom appropriately
dosed diuretics are ineffective)
Colloids: Popular but Controversial
dosed diuretics are ineffective)
� e.g., pulmonary edema or effusion causing respiratory
failure
� Theoretically, loop diuretics (highly protein bound) will
bind to albumin, resulting in reduced efficacy.
Page 2-9
Maintenance IV Fluid
� Not for patients with S/S of intravascular volume
depletion
� When asked for a stat D5W 0.45% NaCl + KCl 20 mEq/L
for a hypotensive patient, consider alternative
� Typical maintenance IV fluid is D5W 0.45% NaCl + KCl
20 – 40meq/L20 – 40meq/L
� Omit KCl if elevated K or kidney failure
� 0.9% NaCl, LR, or colloids are generally not
appropriate maintenance IV fluids
� Exception: Neurologically-injured patients
� Evaluate IV fluids daily
Page 2-10
How much fluid?
� Remember for resuscitation, administer 500 –
1000 mL bolus, then reevaluate.
� Continue until S/S improve
� For daily fluid maintenance, many practitioners
use 1500 mL for first 20kg, then 20 mL/kg use 1500 mL for first 20kg, then 20 mL/kg
thereafter (~ 2500 mL/day)
� Adjust rate based on I/O, estimated insensible loss
(e.g., fever)
� D/C when taking enough oral fluids
Page 2-10
Self-Assessment Question #1: Fluids
� 74 yo female with cough, temp 102, and lethargic
� BP 72/40, HR 115, UO 10 ml/hr, WBC 18K, Cr 1.7
(baseline 1.2), wt 72kg
� After 500 mL NS IV bolus, BP 80/46, HR 113� After 500 mL NS IV bolus, BP 80/46, HR 113
� CXR – pneumonia
� PMH – CAD, arthritis
Page 2-4
Which is the best treatment option?
A. Furosemide 40mg IV
B. 5% albumin 500ml + NE for SBP > 90
C. 1000ml bolus with D5W/.9% NaClC. 1000ml bolus with D5W/.9% NaCl
D. 1000ml bolus with 0.9% NaCl
Page 2-4
Which is the best treatment option?
A. Furosemide 40mg IV
B. 5% albumin 500ml + NE for SBP > 90
C. 1000ml bolus with D5W/.9% NaClC. 1000ml bolus with D5W/.9% NaCl
D. 1000ml bolus with 0.9% NaCl
Page 2-4, 2-48
Plasma Osmolality (Posm)
� Posm ~ 275 – 290 mOsm/kg
� Primary determinant of Posm is sodium salts (hence 2 x 140 = 280 ~ Posm)
� Changes in Posm cause fluid shifts across cell membranesmembranes
� Increased Posm causes cellular dehydration
� Decreased Posm causes cellular swelling
� Can cause permanent neurologic damage
� Major changes in serum sodium can result in changes in Posm
Page 2-12
Osmolarity of IV Fluids
� Isotonic
� No osmotic gradient, no fluid shift
� Hypertonic IV Fluid
� Cell dehydration / shrinkage
Hypotonic IV Fluid� Hypotonic IV Fluid
� Cell overhydration can occur if < 150 mOsm/Kg
� RBC swelling = hemolysis
� Brain cell swelling = cerebral edema / herniation
Page 2-12
Calculate Osmolarity of IV Fluid
0.9% NaCl = 0.9 gm/100 mL = 9 gm/L
MW of NaCl = 58.5 gm/mol
Osmotic Coefficient NaCl = 0.93
9 gm
L
1mol
58.5gm
2 osm
mol
0.931000mosm
1 osm* * * *
= 287 mOsm/L (isotonic)
Page 2-12
Patient Case #3
� 72 yo female with HTN started HCTZ 3 weeks ago,
with dizziness, fatigue, nausea
� Na 116, Wt 60kg, BP 86/50, HR 122
� Which regimen is best?
A. NS 100 mL/hr
B. NS 500 mL bolus
C. 3% NaCl 60 mL/hr
D. 23.4% NaCl 30 mL bolus as needed
Page 2-19
Patient Case #4
� What is the treatment goal for the first 24 hours
in correcting her serum Na? (Initial value is 116
mEq/L)
Goal Na 140A. Goal Na 140
B. Goal Na 132
C. Goal Na 126
D. Maintain 116 – 120
Page 2-19
Symptoms of Hyponatremia
Serum Sodium (mEq/L)
Symptoms
120 – 125 Nausea, malaise120 – 125 Nausea, malaise
115 – 120Headache, lethargy, obtundation,
unsteadiness, confusion
Less than 115 Seizure, coma
Page 2-18
Other Considerations in Hyponatremia
� Hyperglycemia
� Correct hypokalemia first
� Hypokalemia can cause hyponatremia due to an intracellular
shift of Na to maintain electroneutrality
K+ Na+
� As K+ is replaced, serum Na will also increase due to an
extracellullar shift
� Also consider volume status
K Na+
K+ Na+
Page 2-19
Hyponatremia and Volume
Hypervolemic
Hyponatremia
Euvolemic
Hyponatremia
Hypovolemic
Hyponatremia
Example HF SIADH Fluid loss
Treatment
Restrict H20
Underlying Cause
Vaptan
Restrict H20
Underlying Cause
Vaptan
Fluid
resuscitation
Page 2-17
Hypovolemic Hyponatremia
� Hypovolemia is a potent stimulus for ADH secretion
which perpetuates hyponatremia
� When volume restored, ADH secretion slows
� Treat with fluid resuscitation using 0.9% NaCl
Once ADH secretion is reduced, serum Na can rapidly � Once ADH secretion is reduced, serum Na can rapidly
correct
� Careful monitoring is required to prevent overly rapid
correction (a medication error that can cause
permanent neurologic damage!)
Page 2-17
Patient Case #3
� 72 yo female with HTN started HCTZ 3 weeks ago,
with dizziness, fatigue, nausea
� Na 116, Wt 60kg, BP 86/50, HR 122
� Which regimen is best?
A. NS 100ml/hr
B. NS 500ml bolus
C. 3% NaCl 60ml/hr
D. 23.4% NaCl 30ml bolus as needed
Page 2-19
Patient Case #3
� 72 yo female with HTN started HCTZ 3 weeks ago,
with dizziness, fatigue, nausea
� Na 116, Wt 60kg, BP 86/50, HR 122
� Which regimen is best?
↑ ADH
A. NS 100ml/hr
B. NS 500ml bolus
C. 3% NaCl 60ml/hr
D. 23.4% NaCl 30ml bolus as needed
↑ ADH
↓ Na
Page 2-19, 2-45
Here’s an opposite problem:
Hypernatremia in Patient Case # 6
� 74 yo female on Jevity TF’s at 60 ml/hr for 8 days
through PEG, 50kg
� Recent CVA, non-communicative� Recent CVA, non-communicative
� Na 142→149 →156 →163 on days 3→8
� Treatment?
Page 2-21
Hyponatremia and Volume
Hypervolemic
Hyponatremia
Euvolemic
Hyponatremia
Hypovolemic
Hyponatremia
Example HF SIADH Fluid loss
Treatment
Restrict H20
Underlying Cause
Vaptan
Restrict H20
Underlying Cause
Vaptan
Fluid
resuscitation
Page 2-17
Vaptans
� Vasopressin receptor antagonists
� AVP secreted by hypothalamus to regulate
osmolality
� IV conivaptan, oral tolvaptan
� Safe and efficacious for euvolemic (SIADH) or � Safe and efficacious for euvolemic (SIADH) or
hypervolemic hyponatremia (CHF, cirrhosis)
persisting despite fluid restriction
� Facilitate aquaresis (electrolyte-free water excretion)
� Increase Na
� Alleviate symptoms and reduce weight in CHF
Page 2-18
Vaptans
� No evidence of improved clinical outcomes in prospective
randomized controlled studies
� i.e., fall prevention, hospitalization, hospital length of stay, mortality
� Substrates and inhibitors of CYP 450 3A4 isoenzymes, so
monitor for drug interactions
3A4 inhibitors could decrease vaptan metabolism, leading to a rapid � 3A4 inhibitors could decrease vaptan metabolism, leading to a rapid
increase in serum Na
� Fluid restriction in combination with a vaptan during the first
24 hours can also increase risk of overly rapid correction of
serum Na
� Avoid fluid restriction in first 24 hours of vaptan use
Page 2-18
Hypertonic Saline
� Typically 3%, 7.5%, or 23.4%
� Osmolarity ~ 950, 2400, 7400 respectively
� Administer via central line
� Use� Use
� Traumatic Brain/neurologic injury to reduce elevated ICP and/or increase CPP (3%, 7.5%, 23.4%)
� Symptomatic Hyponatremia (usually 3%)
� Usually acute = symptom onset within 3 days
� Symptomatic = lethargy, psychosis, seizure, coma
Page 2-13
Hypertonic Saline is NOT for:
� Chronic asymptomatic hyponatremia
� e.g., SIADH usually chronic and treated with fluid restriction and treating the cause
� Hyponatremia secondary to DKAHyponatremia secondary to DKA
� As glucose is corrected, Na will too
� Hyponatremia associated with CHF
� Usually chronic and asymptomatic
� If symptomatic, caution regarding volume overload with hypertonic saline
Page 2-13
Common Error
� 150 mEq Sodium Bicarbonate mixed in 850 mL IV
Fluid (typically to prevent contrast nephropathy)
� If mixed in 0.9% NaCl, the result is equivalent to
3% sodium (hypertonic)3% sodium (hypertonic)
� Use D5W as admixture instead
� Sterile water could be used as well, but potential for
error
Page 2-15
Safe Use of Hypertonic Saline for
Symptomatic Hyponatremia
� Goal is a SMALL but QUICK rise in Na by 0.75 – 1
mEq/L/hr to a concentration of 120 mEq/L, then
slow to 0.5 mEq/L/hr
� Can be achieved using 3% NaCl 1 – 2 mL/kg/hr or � Can be achieved using 3% NaCl 1 – 2 mL/kg/hr or
250 mL bolus over 30 min
� Treat until:
� Symptoms stop
� Safe, serum Na range (120 – 125 mEq/L)
� Obtained max safe change in serum Na
Page 2-14
Complications of HS:
Avoid Rapid Change in Na+
� Max change is 10 – 12 mEq/L in 24 hours
� Rapid correction of serum sodium can cause central pontine myelinolysis or osmotic demyelination syndromedemyelination syndrome
� Characterized by paraparesis, quadriparesis, coma
� Permanent neurologic damage
� Highest risk is patients with chronic hyponatremia(some things don’t need fixing)
Page 2-15
Patient Case #4
� What is the treatment goal for the first 24 hours
in correcting her serum Na? (Initial value is 116
mEq/L)
Goal Na 140A. Goal Na 140
B. Goal Na 132
C. Goal Na 126
D. Maintain 116 – 120
Page 2-19
Patient Case #4
� What is the treatment goal for the first 24 hours
in correcting her serum Na? (Initial value is 116
mEq/L)
Goal Na 140A. Goal Na 140
B. Goal Na 132
C. Goal Na 126 (a safe range and max change)
D. Maintain 116 – 120
Page 2-19, 2-45
Hypotonic Fluid
� Albumin 25% diluted with SW to make albumin 5% has osmolarity of ~ 60 mOsm/L
� Associated with hemolysis and death
0.225% NaCl (“quarter normal saline”) is � 0.225% NaCl (“quarter normal saline”) is hypotonic with an osmolarity of 68 mOsm/L
� Avoid IV fluid with osmolarity < 150 mOsm/L
Page 2-16
Is hypernatremia a good reason to use
hypotonic saline?
� Generally patients with hypernatremia need water, not NaCl (as in 0.225% NaCl)
� But we NEVER give water IV
If possible, give water by mouth or enterally� If possible, give water by mouth or enterally
� If NPO, give free water IV (D5W)
� Dextrose is metabolized to CO2 and water, so that provides free water and can be given IV
Page 2-16
What to do with those orders for
“quarter normal saline”?� This is a potentially fatal error
� Eliminate risk by changing to:
� D5W (best case scenario if need IV)
� D5W/0.225% NaCl (a recommendation that’s more � D5W/0.225% NaCl (a recommendation that’s more likely to succeed)
� D2.5W/0.225% NaCl (for those who complain about risk of hyperglycemia with 5% dextrose)
� Addition of KCl will also increase osmolarity
� Enteral water (best case scenario)
Page 2-16
Treatment of Hypernatremia
� Rapid correction of chronic asymptomatic
hypernatremia is a potentially fatal medical error.
� In symptomatic hypernatremia, serum Na should
be corrected by no more than 10 – 12 mEq/L/daybe corrected by no more than 10 – 12 mEq/L/day
� Replace water deficit slowly
Page 2-20
Treatment of Hypernatremia
� Estimate water deficit in patients with
hypernatremia:
0.5 to 0.6 x LBW x [(Na/140) -1] for men
0.4 to 0.5 x LBW x [(Na/140) -1] for women
� Replace water deficit slowly following guidelines
for safe changes in serum Na
� If serum Na is decreasing too rapidly, can
administer D5W/0.225% or D5W/0.45% NaCl to
slow rate of decrease
Page 2-21
Hypernatremia in Patient Case # 6
� 74yo female on Jevity TF’s at 60 mL/hr for 8 days
through PEG, 50kg
� Recent CVA, non-communicative
� Na 142→149→156→163 on days 3→8
A. Sterile water IV 80 mL/hr
B. D5W IV 80 mL/hr
C. D5W/0.225% NaCl 80 mL/hr
D. Free water per PEG 200 mL q6 hours
Page 2-21
Hypernatremia in Patient Case # 6
� 74yo female on Jevity TF’s at 60 mL/hr for 8 days
through PEG, 50kg
� Recent CVA, non-communicative
� Na 142→149→156→163 on days 3→8
A. Sterile water IV 80 mL/hr NEVER
B. D5W IV 80 mL/hr option if can’t give enterally
C. D5W/0.225% NaCl 80 mL/hr only if Na ↓ too fast
D. Free water per PEG 200 mL q6 hours enteral first
Page 2-21, 2-45
By the way…
� Hypernatremia in the setting of Case 6 is
completely preventable and should be
considered a medication error
� Can be prevented by being proactive with enteral
administration of water in patients receiving TF’s administration of water in patients receiving TF’s
(especially if 1.5-2 kcal/mL)
� Check the TF label for water content
� Make sure patients receive at least 1 mL water per
calorie administered (will need extra per FT)
� Important in patients who can’t communicate thirst
Page 2-21
Potassium (K+)
� The primary intracellular cation
� Balance K+ between IC and EC compartments is
maintained by:
� β2-stimulation promotes cellular uptake
� Insulin promotes cellular uptake
� Plasma K+ concentration can cause passive shifts in or
out of cells
Page 2-21
Hypokalemia (K+ < 3.5 meq/L)
� Seldom caused by reduced K+ intake because of
↓ kidney excre[on
� Causes of hypokalemia:
� A shift of K+ into cells can occur with
� ↑ pH� ↑ pH
� Insulin or carbohydrate load
� β2 -stimulation (stress, drugs)
� Hypothermia
� GI loss (vomiting, diarrhea, fistula, laxative abuse)
� Urinary loss (diuretics)
� ↓ Mg2+ (increase renal loss of K)
Page 2-22
Treatment Pearls of Hypokalemia
� How much?
� There is no precise calculation of K+ loss based on a
plasma K + concentration
� K + replacement is guided by plasma K +
� How fast?� How fast?
� 10 – 20 mEq/hr, max 20 – 40 mEq/hr requires
continuous EKG monitoring (regardless of route)
� Route?
� Oral KCl should be considered if no symptoms
� If peripheral IV, max concentration is 60 mEq/L
Page 2-22
Treatment Pearls of Hyperkalemia
� Is it real? Does it fit the clinical scenario?
� K+ can be artificially elevated if traumatic venipuncture
(hemolysis)
� Artificially elevated if serum rather than plasma K +
(due to K + release during coagulation)
Is the patient experiencing severe muscle � Is the patient experiencing severe muscle
weakness or EKG changes (peaked t-waves, wide
QRS) or is K+ > 6.5 meq/L (VF can be first sign)?
� No: Consider Kayexalate
� Yes: Urgent treatment
Page 2-23
Urgent Treatment of Hyperkalemia
1. Calcium gluconate 1 – 2 g IV over 2 – 10 minutes
can prevent hyperkalemia-induced arrhythmias
2. Drugs that cause an intracellular shift of K+:
� Insulin 10 units IV (with glucose to prevent
hypoglycemia) – effect within 60minhypoglycemia) – effect within 60min
� Sodium bicarbonate 50 mEq – effect within 30 – 60 min
although efficacy is disputed
� Albuterol (β2 agonist) – effect within 90 min inhaled;
40% won’t respond; consider use in combination with
insulin
Page 2-24
After Urgent Treatment
� Diure[cs to ↑ renal excre[on (if kidneys
functioning)
� Cation-exchange resin (kayexalate) PO or as
retention enema retention enema
� Dialysis
Page 2-24
Focus on Kayexalate & Sorbitol
� Many reports to FDA of bowel injury with both oral
and rectal administration of kayexalate mixed in
sorbitol
� Linked to deposition of drug crystals in GI tract, damaging
mucosa and causing necrosismucosa and causing necrosis
� Most reports involve 70% sorbitol, not 33% (current
premixed suspension)
� Risk of colonic necrosis is rare with 33% formulation
� Caution in kidney or heart failure due to Na
retention
Page 2-25
More Dirt on Kayexalate
� No controlled trials demonstrate efficacy
� Approved in 1958 before FDA required to
demonstrate efficacydemonstrate efficacy
� A recent systematic review found that sodium
polystyrene without sorbitol is also associated
with gastrointestinal injury
Harel Z et al. Am J Med 2013 Page 2-25
More on Calcium use in Hyperkalemia
� Calcium gluconate can be administered peripherally
and is preferred over calcium chloride because of
reduced risk of tissue necrosis
� 10mL of 10% = 1gm (90mg elemental Ca)
� Calcium chloride can be used if central IV access is � Calcium chloride can be used if central IV access is
available, but adjust dose
� 10mL = 1gm (270mg elemental Ca)
� Calcium will not reduce K
� Avoid calcium if digoxin used (↑ risk dig toxicity)
Page 2-24
Replacement of Other Electrolytes pg 2-26 – 2-28
Clinical Pearls
Mg •Oral Mg limited by diarrhea
•If symptomatic (tetany, seizure, HTN), administer 1 – 4gm IV
slowly (1g/hr) to avoid hypotension and/or increased renal
excretion; if torsades can give IV push
PO4 •Major cause of low phosphorus is refeeding syndrome; also PO4 •Major cause of low phosphorus is refeeding syndrome; also
during treatment of DKA
•Prevent refeeding syndrome by supplementing with 10-30
mmol/L IV (↑ risk if malnourished, alcoholism, DKA)
•Oral is poorly absorbed
Ca •Don’t treat (or use PO) if asymptomatic hypocalcemia
associated with low albumin
•Asymptomatic hypocalcemia can be treated with oral calcium
•Don’t give CaCl via peripheral IV (limb ischemia)
Electrolyte Shortages
� Phosphate shortage (2-27)
� Reserve for pediatric and neonatal patients
� Reserve for DKA, refeeding syndrome, ICU patients
� IV fat emulsions contain 15 mmol/L as egg
phospholipidphospholipid
� Calcium shortage (2-28)
� If no gluconate, don’t add Ca chloride to PN
� Use multi-electrolyte products
� Unknown if can dilute Ca chloride and administer
peripherally
Enteral Nutrition: Indication
� Used in hemodynamically stable patients at risk
of malnutrition in whom it is anticipated that oral
feedings will be inadequate for at least 1 – 2
weeksweeks
� Most well-nourished adults without excessive
metabolic stress can tolerate little to no nutrition
for up to 7 days
Page 2-29
Enteral Nutrition - Delivery
� Gastric vs. duodenal feeding tubes
� Improved tolerance with duodenal
� Reduced risk of aspiration with duodenal
� Duodenal tubes clog easier
Must use continuous infusion (not bolus) for duodenal � Must use continuous infusion (not bolus) for duodenal
feeding
� Continuous infusion is most common in
hospitalized patients
� Reduced risk of aspiration compared to bolus feedings
Page 2-29
Enteral Formulations
� Intact or polymeric formulas used for normal
digestive processes
� Elemental formulas used for malabsorptive
processes (e.g., short bowel)processes (e.g., short bowel)
� Typically 1 – 2 kcal/ml
� Specialty formulas
� Renal: concentrated, reduced protein/lytes
� Pulmonary: more fat and fewer carbohydrates
� Diabetic: more fat, fewer carbohydrates, fiber
Page 2-30
Enteral Nutrition Example
A 60kg patient requires ~25 kcal/kg
60kg x 25 kcal/kg = 1500 kcal
Ultracal provides 1 kcal/ml
1500/24 = 62.5 ml/hr1500/24 = 62.5 ml/hr
Start Ultracal at 20 ml/hr and advance every 4-6
hours as tolerated to a goal rate of 62 ml/hr (can
round to 60 or 65)
Page 2-32
Enteral Nutrition:
Don’t forget to add water
� Ultracal provides 830 mL water/L, therefore if
infusing 1500 kcal/day, need to add ~250 mL infusing 1500 kcal/day, need to add ~250 mL
water extra daily
� Order 60 – 70 mL water per feeding tube every 6
hours
Page 2-32
Complications of EN� Aspiration pneumonia
� HOB 30 – 45 degrees
� Hold if gastric residuals are > 250 – 500ml
� Recent evidence shows monitoring without measuring residuals
is safe (no difference in VAP)
� Consider pro-motility agents� Consider pro-motility agents
� Duodenal feedings
� Diarrhea
� More common with higher osmolarity enteral feedings
� Consider other causes (antibiotics, infection, lactose
intolerance, magnesium, sorbitol, etc)
Page 2-31Reignier et al. JAMA 2013: 249-56.
Pro-Motility Agents
� Metoclopramide 5 – 20mg IV q6h
� Erythromycin 250mg IV q6-8h x 72 hours or until
tolerating EN x 24 htolerating EN x 24 h
� Can combine, but monitor for diarrhea
� Avoid prolonged use or prophylactic use due to
increase risk of adverse effects
Page 2-31
Enteral vs. Parenteral
� If the gut works, use it
� Enteral feedings maintains integrity of GI mucosa
and can prevent bacterial translocation
� Early enteral feeding improves outcomes in surgery � Early enteral feeding improves outcomes in surgery
patients.
� No evidence that early parenteral feeding improves
outcomes.
� PN if unable to feed at least 7 days with a
nonfunctioning or inaccessible GI tract
Page 2-33
Premixed PN� 2-compartment bags containing AA in one
compartment and dextrose in other are available
in U.S. (Clinimix; has electrolytes)
� Lipid can be added to container following mixing
compartments or can be administered by Y-site
ProcalAmine contains AA (3%), glycerin (4.3
Miller SJ. Nutr Clin Pract. 2009;24:459-469
� ProcalAmine contains AA (3%), glycerin (4.3
kcal/g), and electrolytes in a single container
does not meet needs of most patients due to
insufficient protein and calories
� Insufficient evidence to show that customized PN
is superior to standardized pre-mixed
Page 2-34
Premixed PNPros
� Fewer manipulations
� ↓ risk contamination
� ↓ compounding errors
� ↓ labor costs
Cons
� Still need additives (MVI, TE)
� Poor if fluid restriction
� Poor if high protein needs
Miller SJ. Nutr Clin Pract. 2009;24:459-469
� Good fit for stable pts
� Non-electrolyte formula available
� Good when AA shortage
needs
� Only 1 or 2 L bags, so standardized admin times problematic
� Clinimix uses CaCl
� Additive stability
� Not breaking sealPage 2-34
Developing a PN Regimen
1. Calories: 25 – 35 kcal/kg/day
� Applies to EN too
� Role of permissive underfeeding
� If BMI > 30, give 22 – 25 kcal/kg based on IBWIf BMI > 30, give 22 – 25 kcal/kg based on IBW
2. Fluid
� Typically 2500 – 3500 mL/day for maintenance
� Do not use PN for fluid resuscitation
Page 2-35
3. Protein 0.8 – 2 g/kg/day
� Less protein if not dialyzed, more if dialysis
� Consider kcal from protein (4 kcal/g)
� Protein buffers 3-in-1’s so keep at 2.5 – 4%
4. Provide about 20-30% of calories as lipid (~10
Developing a PN Regimen
4. Provide about 20-30% of calories as lipid (~10
kcal/g)
5. Provide rest of calories as dextrose (3.4 kcal/g)
� Infuse no faster than 4-6 mg/kg/min (adults only)
� Closer to 4 in patients with hyperglycemia
Page 2-36
Central PN: 70kg Patient
� Total kcal 30 kcal/kg 2100 kcal
� Protein 1.5 g/kg 105 g (420 kcal)
� Lipid 25-30% of total 500 kcal
2100
� Dextrose: 1180 kcal / 3.4 kcal /g ~ 350 g
2100-420-5001180
Page 2-37
Peripheral PN
� Central PN is guided by patient’s nutritional
needs
� Peripheral PN is guided by final concentration of
dextrose and amino acids in formula to maintain
osmolarity < 900 mOsm/Losmolarity < 900 mOsm/L
� Dextrose 10% or less
� AA 2.5 – 4%
� Electrolyte restrictions
� Calcium < 5 mEq/L
� K < 40 mEq/L
Page 2-33
Calcium – Phosphate Precipitation
� Risk is low if Ca < 6 mEq/L & Phos < 30 mmol/L
� Calcium chloride precipitates > calcium gluconate
� Final AA should be at least 2.5%
� Forms soluble complexes with Ca and Phosphorus
� Buffer to maintain a lower pH to prevent precipitation � Buffer to maintain a lower pH to prevent precipitation
� As temp ↑, so does risk (refrigerate)
� Filters decrease risk of embolism (0.22 for 2-in-1, or
1.2 for 3-in-1)
� Phosphate is first electrolyte added, then mix well,
then add Ca last
Page 2-39
Complications of PN
� Catheter-related infection (S. aureus, C. albicans)
� Gut atrophy is linked to bacteremia
� Overfeeding
� Hepatic steatosis� Hepatic steatosis
� Hypercapnia
� Hyperglycemia
� Azotemia
� EFAD (impaired wound healing) if no lipid for
~ 1 – 3 weeks
Page 2-39
Complications of PN� Refeeding syndrome in acutely or chronically
malnourished patients
� Reductions in Phos, K, Mg
� Cardiac and respiratory dysfunction
� Patients at risk (anorexia, alcoholism, cancer,
chronically ill, poor intake x 1 – 2 wks, wt loss)chronically ill, poor intake x 1 – 2 wks, wt loss)
� Prevent by initially infusing < 50% of calories and
advancing over several days to goal
� Provide more Phos, K, Mg initially, monitor daily
and replace as needed
Page 2-40
Monitoring PN
� Infection – temp, WBC, site
� Fluid – wt, edema, vitals, in/out, temp
� Prealbumin is useful for chronic nutrition support
in patients who are not critically ill (normal 16-40
mg/dL)mg/dL)
� Blood glucose
� Electrolyte and acid-base status
� TG (withhold lipid if > 400 mg/dL)
� Readiness for enteral or oral nutrition
Page 2-41
Thank You!
Leslie A. Hamilton, PharmD, BCPS
Assistant ProfessorAssistant Professor
University of Tennessee Health Science
Center College of Pharmacy
Department of Pharmacy Practice
lhamilt4@uthsc.edu
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